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PubMed1994

Dose response of succinylcholine at the adductor pollicis of children with cerebral palsy during propofol and nitrous oxide anesthesia.

Children with cerebral palsy may be resistant to paralysis induced by nondepolarizing neuromuscular blocking drugs. Potency of a bolus of succinylcholine in children with cerebral palsy has not been studied previously. Therefore, we measured the response of the adductor pollicis to succinylcholine in children with cerebral palsy anesthetized with propofol and nitrous oxide. Forty children between the ages of 2 and 10.2 yr with spastic quadriplegic cerebral palsy were randomly assigned to receive 100, 175, 250, or 375 micrograms/kg of succinylcholine during anesthesia with propofol and nitrous oxide. The ulnar nerve was stimulated with a train-of-four supramaximal stimulus every 10 s and the compound electromyogram of the adductor pollicis recorded by a Datex NMT monitor. Plasma cholinesterase activity was measured in all patients with three different substrates (propionylthiocholine, benzoylcholine, and succinylcholine). Dibucaine number was also determined using inhibition of benzoylcholine degradation. ED50 of succinylcholine was 146.8 micrograms/kg with 95% confidence intervals of 111.4-193.7 micrograms/kg. ED95 of succinylcholine was 360.5 micrograms with 95% confidence intervals of 273.3-475.5 micrograms/kg. We conclude that children with cerebral palsy are slightly sensitive to succinylcholine, but probably not sufficiently to be clinically important.

Anesthesia, General↗
PubMed2003

Postoperative myalgia after succinylcholine: no evidence for an inflammatory origin.

UNLABELLED: A common side effect associated with succinylcholine is postoperative myalgia. The pathogenesis of this myalgia is still unclear; inflammation has been suggested but without convincing evidence. We designed the present study to investigate whether an inflammatory reaction contributes to this myalgia. The incidence and severity of succinylcholine-associated myalgia was determined in 64 patients pretreated with saline or dexamethasone before succinylcholine (n = 32 for each). Incidence and severity of myalgia did not differ significantly between the two groups: 15 patients in the dexamethasone group complained of myalgia compared with 18 patients in the saline group, and severe myalgia was reported by five patients and three patients, respectively (not significant). At 48 h after surgery, 12 patients in both groups still suffered from myalgia (not significant). In addition, interleukin-6 (IL-6) as an early marker of inflammation was assessed in a subgroup of 10 patients pretreated with saline. We found an increase of IL-6 for only three patients, but only one patient reported myalgia; no relationship between myalgia and the increase of IL-6 was found. In conclusion, there is no evidence for an inflammatory origin of succinylcholine-associated myalgia. IMPLICATIONS: Administration of dexamethasone before succinylcholine was not effective in decreasing the incidence or the severity of succinylcholine-induced postoperative myalgia. Furthermore, there was no significant relationship between postoperative myalgia and time course of interleukin-6 concentrations, a marker of inflammation. Pretreatment with dexamethasone is not justified to prevent postoperative myalgia after succinylcholine.

Adult↗
PubMed1993

Neuromuscular and hemodynamic effects of mivacurium and succinylcholine in adult patients during nitrous oxide-propofol-fentanyl anesthesia.

The neuromuscular and hem+odynamic effects of mivacurium 0.15 mg/kg and succinylcholine 1 mg/kg were compared in 26 adult patients (ASA I and II) during nitrous oxide-oxygen-propofol-fentanyl anesthesia. Neuromuscular block was monitored by recording the compound electromyogram of the hypothenar muscle resulting from supramaximal train-of-four stimuli applied to the ulnar nerve. Time to onset of over 95% block and duration to 25% recovery of control twitch after injection of mivacurium were significantly longer than for succinylcholine (201 +/- 37.6 vs 54 +/- 5.2 sec and 13.0 +/- 2.2 vs 8.4 +/- 2.1 min; mean +/- SD). Onset of mivacurium with priming technique was shortened (125 +/- 20.7 sec), but was also slower than that of succinylcholine. Although the recovery index during spontaneous recovery was significantly longer for mivacurium than for succinylcholine (6.9 +/- 1.3 vs 5.1 +/- 0.9 min), antagonism with neostigmine at 25% recovery of twitch height sufficiently facilitated the recovery index of mivacurium (4.5 +/- 1.0 min) to a level similar to that of succinylcholine with no statistical difference. The hemodynamic effects of mivacurium were few as compared to those of succinylcholine. In conclusion, mivacurium is considered to have additional advantages for short procedures when succinylcholine is undesirable.

Adult↗
PubMed1984

Shelf life of unrefrigerated succinylcholine chloride injection.

The shelf life of succinylcholine chloride injection at several pH values when stored at room temperature was evaluated. Solutions containing 20 mg/ml of succinylcholine chloride were stored at 25 and 40 degrees C. The reaction was studied at pH values ranging from 3.0 to 4.5. At two-week intervals, the solutions were assayed by high-pressure liquid chromatography. The initial amount of succinylcholine chloride in all samples was 100.1 +/- 2.37% of label claim. Hydrolysis of succinylcholine chloride in unbuffered solutions followed apparent zero-order kinetics. The pH range of maximum stability was found to be from 3.75 to 4.50. Succinylcholine chloride decomposed at a considerably higher rate at 40 degrees C. Allowing for the effects of pH adjustment during manufacture and degradation during shipping, losses of 7.0% and 9.0% potency can be expected after storage at 25 degrees C for four and six weeks, respectively. Succinylcholine Chloride Injection, USP, should be stored in the refrigerator; if unbuffered succinylcholine chloride injection complying with USP pH limits must be stored at room temperature, it should not be kept for longer than four weeks.

Drug Stability↗
PubMed1983

Succinylcholine-induced increases in plasma catecholamine levels in humans.

Given the hypothesis that interaction of succinylcholine with nicotinic receptors releases endogenous catecholamines, plasma levels of epinephrine and norepinephrine were determined in anesthetized and manually ventilated patients immediately before and 2 min after intravenous administration of succinylcholine. Anesthesia was induced with intravenous thiopental (3-4 mg/kg) followed by the administration of nitrous oxide and oxygen (1:1) and 0.5-1.0% halothane. Stimulation of the patients was avoided. Succinylcholine (1 mg/kg) or metocurine (0.3 mg/kg) was injected intravenously and ventilation was controlled without intubation. Plasma norepinephrine levels increased from 301 pg/ml to 491 pg/ml (SEM = +/- 19 pg/ml, P less than 0.01, N = 5) 2 min after the injection of succinylcholine; the increase in plasma epinephrine was not statistically significant. The time course of catecholamine elevation was studied in three additional patients. The increase of norepinephrine occurred immediately after the injection of succinylcholine, peaked (647 +/- 67 pg/ml) around the third minute, and disappeared by the 10th min. The increase in epinephrine was less marked. Plasma levels of catecholamines did not change after the injection of metocurine (N = 2). The possibility that succinylcholine stimulates nicotinic receptors on the postganglionic sympathetic terminals is discussed. We propose that the elevation of plasma norepinephrine might contribute to the development of early adverse cardiovascular reactions to succinylcholine.

Adult↗
PubMed1990

Succinylcholine-induced increases in CSF pressure are not affected by PaCO2 or mean arterial pressure in dogs.

The effects of PaCO2 and mean arterial pressure (MAP) on succinylcholine-induced changes in cerebrospinal fluid (CSF) pressure were examined in 31 dogs anesthetized with halothane (0.7% end-expired) and nitrous oxide (66% inspired) in oxygen. Group 1 (n = 9) received succinylcholine (1.5 mg/kg i.v.) without control of PaCO2 or MAP. Group 2 (n = 12) received succinylcholine with CO2 maintained at control, and no regulation of MAP. Group 3 (n = 10) received succinylcholine without regulation of PaCO2 and maintenance of MAP at control values with trimethaphan. Succinylcholine produced an increase in CSF pressure of 1.7 +/- 1.7-3.9 +/- 3.6 cm H2O (mean +/- SD). There were no differences in CSF pressure increase between groups. The increase in CSF pressure was compared to the variation in the uncontrolled physiological parameter (i.e., CSF pressure was compared to PaCO2 and MAP in group 1, MAP in group 2, and PaCO2 in group 3). The CSF pressure increase over time did not strictly parallel changes in PaCO2 and/or MAP, and the magnitude of increase of CSF pressure did not correlate significantly with PaCO2 and/or MAP. It is concluded that, in anesthetized dogs, succinylcholine produces relatively small increases in CSF pressure whether or not PaCO2 or MAP is controlled. These results do not support the hypothesis that a succinylcholine-induced increase in CSF pressure is due chiefly to an increase in PaCO2 and/or MAP and can be abolished by preventing those changes.

Journal Article↗
PubMed1999

Organophosphorus pesticide-induced butyrylcholinesterase inhibition and potentiation of succinylcholine toxicity in mice.

Succinylcholine is the most important rapid-acting depolarizing muscle relaxant during anesthesia. Its desirable short duration of action is controlled by butyrylcholinesterase, the detoxifying enzyme. There are two reported cases of prolonged paralysis from succinylcholine in patients poisoned with the organophosphorus insecticides parathion and chlorpyrifos. The present study examines the possibility that other organophosphorus and methylcarbamate pesticides might also prolong succinylcholine action by inhibiting butyrylcholinesterase using mice treated intraperitoneally as a model and relating inhibition of blood serum hydrolysis of butyrylthiocholine to potentiated toxicity (mouse mortality). The organophosphorus plant defoliant tribufos (4 h pretreatment, 160 mg/kg) and organophosphorus plant growth regulator ethephon (1 h pretreatment, 200 mg/kg) potentiate the toxicity of succinylcholine by seven- and fourfold, respectively. Some other pesticides or analogs are more potent sensitizers for succinylcholine toxicity with threshold levels of 0.5, 1.0, 1.7, 8, 10, and 67 mg/kg for phenyl saligenin cyclic phosphonate, profenofos, methamidophos, tribufos, chlorpyrifos, and ethephon, respectively. Enhanced mortality from succinylcholine is generally observed when serum butyrylcholinesterase is inhibited 55-94%. Mivacurium, a related nondepolarizing muscle relaxant also detoxified by butyrylcholinesterase, is likewise potentiated by at least threefold on 4 hour pretreatment with tribufos (25 mg/kg) or profenofos (10 mg/kg).

Animals↗
PubMed1979

Effect of pancuronium on intraocular pressure changes induced by succinylcholine.

The study was undertaken to evaluate the influence of pretreatment with a small dose of pancuronium on intraocular pressure changes associated with administration of succinylcholine and tracheal intubation. Thirty patients divided into control and study groups were anaesthetized with sodium thiopentone (3-5 mg mg.kg-1) and intubation with the aid of succinylcholine (1 mg.kg-1). The control group received saline pretreatment while the study group received pancuronium 1 mg three minutes before succinylcholine. Anaesthesia was maintained with nitrous oxide and oxygen (70:30). A Schiotz tonometer was used to measure intraocular pressure before induction of anaesthesia, one minute after succinylcholine and immediately after intubation. Patients in the control group demonstrated significant elevation of intraocular pressure at one minute after succinylcholine and immediately after intubation, while the study group showed no significant change at the same observation periods. These findings indicate that pretreatment with pancuronium 1 mg three minutes before succinylcholine may be beneficial in patients with high intraocular pressure and penetrating injuries of the eye.

Adolescent↗
PubMed1977

Dual action of pancuronium on succinylcholine block.

The effects of pretreatment with both sub-paralyzing and paralyzing doses of pancuronium and d-tubocurarine, on the onset and duration of succinylcholine-induced neuromuscular blockade were evaluated and compared in 225 patients. D-tubocurarine antagonized both onset and duration of succinylcholine block, while pancuronium produced a dual effect, antagonizing the onset and potentiating the duration of succinylcholine block. Pretreatment with d-tubocurarine (0.07 mg/kg, 0.3 mg/kg and 0.6 mg/kg) increased the time to onset of succinylcholine paralysis from 28 to 118%, and decreased the duration from 16 to 37%. Pancuronium (0.02 mg/kg, 0.04 mg/kg and 0.08 mg/kg) also antagonized the onset of succinylcholine paralysis with increases of 32 to 114%, but potentiated its duration from 30 to 103% compared with succinylcholine alone in the same patients. Although pancuronium markedly inhibited serum cholinesterase in vitro (I50=5 X 10(-7) mol) there was only a 10% inhibition of cholinesterase in vivo after pancuronium 0.08 mg/kg.

Adult↗
PubMed1981

The effect of intravenous diazepam on rise of intraocular pressure following succinylcholine.

Because succinylcholine raised intraocular pressure, its use to facilitate tracheal intubation for ocular surgery, especially in emergency open-eye cases, has been a controversial topic among anaesthetists for more than two decades. In recent years, intravenous diazepam pretreatment before succinylcholine has been reported to reduce the untoward side effects of myalgia, and elevation of serum potassium and creatine phosphokinase. This study was designed to assess the effect of pretreatment with intravenous diazepam 0.1 mg kg-1 on control (base-line) intraocular pressure and to determine if such pretreatment diminished the rise in intraocular pressure following the standard anaesthesia induction sequence of thiopentone 3 - 5 mg kg-1., followed by tracheal intubation. Such diazepam pretreatment was shown to reduce the intraocular pressure from control levels and to diminish the rise of intraocular pressure following succinylcholine and tracheal intubation. Because succinylcholine produces rapid onset of neuromuscular block for tracheal intubation and since only minor intraocular pressure elevation occurs following thiopentone and succinylcholine in patients pretreated with diazepam, its use in ocular surgery, including emergency open-eye cases, can be rationally advocated. The addition of 0.6 mg kg-1 d-tubocurarine to the diazepam pretreatment did not produce a further reduction of the increase of intraocular pressure following succinylcholine.

Adult↗
PubMed1983

The heart rate response to succinylcholine in children: a comparison of atropine and glycopyrrolate.

To determine whether intravenous atropine and glycopyrrolate are equally effective in preventing succinylcholine-induced heart rate changes, we studied the heart rate during the first 78 seconds of anaesthesia in 40 children anaesthetized with either thiopentone, atropine (0.02 mg X kg-1) and succinylcholine (2 mg X kg-1), or thiopentone, glycopyrrolate (0.01 mg X kg-1) and succinylcholine (2 mg X kg-1). Each treatment group was divided into four subgroups which differed only in the interval (6, 10, 15, 20 seconds) between injection of atropine or glycopyrrolate and succinylcholine. During the 54 seconds after succinylcholine, the mean heart rate of each subgroup decreased transiently and then returned to the pre-induction heart rate or higher. There was no difference in either the magnitude or the duration of the decrease in heart rate or the subsequent increase in heart rate between respective subgroups. Bradycardia occurred in only two patients, both of whom received glycopyrrolate. We conclude that atropine (0.02 mg X kg-1) and glycopyrrolate (0.01 mg X kg-1) are equally effective in attenuating succinylcholine-induced changes in heart rate in children.

Anesthesia, General↗
PubMed1995

It is not necessary to administer more than 10 micrograms.kg-1 of atropine to older children before succinylcholine.

It is common practice at the Hospital for Sick Children, Toronto, to administer atropine 20 micrograms.kg-1 prior to succinylcholine in infants and children. It is unclear whether "prophylactic" administration of this dose of atropine to older children (6-16 yr) is necessary. This study was designed to compare the changes in heart rate, rhythm and mean arterial pressure after administration of either atropine 10 or 20 micrograms.kg-1 with succinylcholine or vecuronium (control group) to older children anaesthetized with thiopentone. Thirty-six ASA I or II patients (6-16 yr) were studied. Anaesthesia was induced with thiopentone 5 mg.kg-1. Patients were randomly assigned to receive: (a) atropine 10 micrograms.kg-1 and succinylcholine 1.5 mg.kg-1 (n = 12), (b) atropine 20 micrograms.kg-1 and succinylcholine 1.5 mg.kg-1 (n = 13) or (c) vecuronium 0.1 mg.kg-1 (n = 11) to facilitate tracheal intubation. Heart rate and rhythm were recorded continuously using a computerised analogue interface whereas blood pressure was monitored non-invasively before induction of anaesthesia, immediately before and at one and three minutes after laryngoscopy. No difference was observed between patients who received atropine 10 or 20 micrograms.kg-1 prior to succinylcholine. No episode of sinus bradycardia occurred. Premature atrial contractions were observed in two patients (one succinylcholine/atropine 20 micrograms.kg-1, one vecuronium). Administration of atropine 20 micrograms.kg-1 prior to succinylcholine provides no advantage over atropine 10 micrograms.kg-1 in older children in terms of cardiovascular stability.

Adolescent↗
PubMed1986

The effects of atracurium on intraocular pressure during steady state anaesthesia and rapid sequence induction: a comparison with succinylcholine.

The effects of atracurium 0.5 mg X kg-1 or succinylcholine 1.0 mg X kg-1 on intraocular pressure (IOP) were studied in ten patients during steady state nitrous oxide-oxygen-fentanyl anaesthesia. IOP was unchanged following atracurium but, one minute after succinylcholine, it had increased significantly (p less than 0.025) from 5.6 mmHg to 13.2 mmHg and remained significantly above control for 3 min. Twenty additional patients received either atracurium 0.75 mg X kg-1 or succinylcholine 1.0 mg X kg-1 as part of a rapid sequence induction, atracurium being administered prior to, and succinylcholine after, thiopentone. Intubating conditions were acceptable in all patients in both groups. Administration of thiopentone was associated with a significant (p less than 0.025) decrease in IOP. Although IOP increased in both groups as a result of laryngoscopy and intubation (from 8.0 mmHg to 12.1 mmHg in the atracurium Group and from 7.5 mmHg to 14.5 mmHg in the succinylcholine group) it did not exceed pre-induction IOP in the former. In the succinylcholine group, IOP after intubation exceeded pre-induction values for 2 min, although this increase was significant (p less than 0.05) only at the immediate post-intubation reading. It is concluded that atracurium in a dose of 0.75 mg X kg-1 is a suitable relaxant for use in rapid sequence induction.

Anesthesia, Endotracheal↗
PubMed1985

Atracurium for short surgical procedures: a comparison with succinylcholine.

A comparison was made between atracurium and succinylcholine in 40 patients undergoing short gynaecological procedures of 30 minutes or less. Good intubating conditions were produced in 76.7 +/- 39.3 seconds (mean +/- S.D.) with succinylcholine 1 mg . kg-1 and 198 +/- 84 seconds with atracurium 400 micrograms . kg-1. Muscle relaxation was maintained with the initial dose of atracurium or with repeated boluses of succinylcholine. The mean time of surgery was 17.65 +/- 5.3 minutes in the atracurium group and 15.2 +/- 4.6 minutes in the succinylcholine group. Residual neuromuscular block with atracurium was reversed with neostigmine 0.036 mg . kg-1 and atropine 0.018 mg . kg-1. Recovery of neuromuscular function following reversal, assessed by return of all responses to train-of-four stimulation occurred in 5.05 +/- 4.6 minutes in the atracurium group but half the above doses of neostigmine and atropine were repeated in three patients. We conclude that a single dose of atracurium 400 micrograms . kg-1 is suitable for intubation and maintainance of muscle relaxation for short surgical procedures. However, the onset of action is slow, compared to succinylcholine. Residual neuromuscular block can be antagonised with standard doses of neostigmine, less than 20 minutes after the initial dose of relaxant. Atracurium appears to be a suitable alternative for short procedures where succinylcholine is unsuitable or contraindicated.

Adolescent↗
PubMed1998

Propofol reduces succinylcholine induced increase of masseter muscle tone.

PURPOSE: Succinylcholine is known to increase the tone of the masseter muscles. As excessive jaw tension may complicate rapid sequence induction, we investigated three induction techniques, all including the use of succinylcholine, with respect to masseter muscle tone, neuromuscular blockade, intubation conditions, and time course of intubation. METHODS: Sixty adult patients were allocated to one of three induction groups: Group THIO received 5 mg.kg-1 thiopentone, Group THIO/ATR received 5 mg.kg-1 thiopentone plus 0.05 mg.kg-1 atracurium for precurarization, and Group PROP received 2.5 mg.kg-1 propofol. All patients received 3 micrograms.kg-1 fentanyl and 1.5 mg.kg-1 succinylcholine. Time for induction of anaesthesia was recorded, and, after inserting a Grass Force Transducer between upper and lower incisors, jaw tone and the time course of jaw tension was recorded before and after the administration of succinylcholine. RESULTS: No differences in the onset of sleep were observed among the three groups (Group THIO 33 +/- 2 sec: THIO/ATR 30 +/- 2 sec: PROP 35 +/- 2 sec, mean +/- SE). Masseter preloads following induction of anaesthesia were similar in all three groups (THIO 16.4 +/- 2.1 N: THIO/ATR 15.1 +/- 2.0 N: PROP 12.7 +/- 1.6 N). However, after administration of succinylcholine, the increase in masseter tone was less in Groups PROP (5.0 +/- 1.1 N) and THIO/ATR (6.4 +/- 2.1 N) than in Group THIO (12.4 +/- 3.0 N; P < 0.05). CONCLUSION: Jaw tension after administration of succinylcholine is influenced by the choice of induction agent. The increase of masseter muscle tone is lower following propofol or thiopentone/atracurium induction than with thiopentone alone.

Adolescent↗
PubMed1986

Augmentation of succinylcholine-induced neuromuscular blockade by calcium channel antagonists.

The block of endplate currents (EPCs) by succinylcholine, in frog cutaneous pectoris muscles, is significantly potentiated by certain organic calcium channel antagonists, at concentrations at which the calcium channel antagonists have no effect on EPCs themselves. Succinylcholine alone blocked the current in a dose-dependent manner with an IC50 = 2.7 microM in voltage-clamped muscle fibers. The ability of succinylcholine to block endplate currents was potentiated by nicardipine (3.5- and 31-fold by 1 and 10 microM, respectively), by bepridil (4.3-fold by 1 microM), and by verapamil (7.7-fold by 10 microM). The dihydropyridine nifedipine (10 microM), did not potentiate the succinylcholine effect. Since the calcium channel antagonists do not affect endplate currents directly at these concentrations, a channel blocking or receptor antagonistic effect of these drugs is not indicated. We therefore suggest that the enhancement of block by succinylcholine may be due to the increased desensitization of the receptor. Furthermore, this enhancement of desensitization may explain the effects of these calcium channel antagonists seen in whole animal studies, where the contractures caused by acetylcholine and succinylcholine, applied systemically, are blocked.

Animals↗
PubMed1996

A mixture of mivacurium and rocuronium is comparable in clinical onset to succinylcholine.

STUDY OBJECTIVES: To compare the clinical onset and duration of a combination of mivacurium and rocuronium with succinylcholine, and to determine the efficacy of this mixture for rapid tracheal intubation. DESIGN: Observer-blind prospective study. SETTING: Teaching hospital. PATIENTS: 70 ASA status I and II patients having general anesthesia for elective surgery. MEASUREMENTS AND MAIN RESULTS: After induction of general anesthesia, patients randomly received succinylcholine 1.0 mg/kg, rocuronium 0.6 mg/kg, or a combination of rocuronium 0.6 mg/kg and mivacurium 0.15 mg/kg. Evoked muscular response at the adductor pollicis was measured by mechanomyography. The time from injection of muscle relaxant(s) to ablation of T1 (clinical onset) and recovery of T1 to 25% of control height (clinical duration) was recorded. Intubating conditions 45 seconds after administration of muscle relaxants were assessed. There was no significant difference in clinical onset time between succinylcholine (mean +/- SD, 47.4 +/- 6.5 seconds) and the combination of mivacurium-rocuronium (51.2 +/- 13.4 seconds). Intubating conditions with mivacurium-rocuronium were comparable to those of succinylcholine. The clinical duration of rocuronium 0.6 mg/kg (38.9 +/- 12.3 minutes) was prolonged by the addition of mivacurium (49.0 +/- 9.6 minutes). CONCLUSIONS: This combination of mivacurium and rocuronium is comparable to succinylcholine in both clinical onset time and quality of intubating conditions. When rapid onset of dense neuromuscular blockade and intermediate clinical duration is desirable, this mixture may be an acceptable alternative to succinylcholine.

Adjuvants, Anesthesia↗
PubMed1999

Intraocular pressure changes during rapid sequence induction and intubation: a comparison of rocuronium, atracurium, and succinylcholine.

STUDY OBJECTIVE: To compare changes in intraocular pressure (IOP) during rapid sequence induction and intubation following rocuronium, succinylcholine, and atracurium. DESIGN: Open-label, prospective, randomized study. SETTING: Operating room at the Eye Foundation Hospital (University of Alabama at Birmingham) PATIENTS: 45 ASA physical status I, II, and III patients, aged 18 to 65 years, scheduled for elective eye surgery with general anesthesia. INTERVENTIONS: Anesthesia was rapidly induced in unpremedicated patients with a fixed combination of midazolam 0.025 mg/kg, alfentanil 0.025 mg/kg, and propofol 1.5 mg/kg. Intubation was performed, as clinically indicated, approximately 60 seconds following administration of rocuronium 0.6 mg/kg, atracurium 0.5 mg/kg, or succinylcholine 1 to 1.5 mg/kg. MEASUREMENTS AND MAIN RESULTS: Intraocular pressure was measured before induction of anesthesia (baseline), following anesthesia induction and administration of muscle relaxant (before intubation), and after intubation. The percent change in IOP from baseline was significantly decreased in the rocuronium group compared with the succinylcholine group (p = 0.046) before intubation. This trend continued after intubation, but the difference was no longer significant (p = 0.070). Intubation scores for rocuronium and succinylcholine groups were similar, and both scores were superior to that for the atracurium group (p = 0.002). CONCLUSION: Intraocular pressure can be controlled during emergency induction of anesthesia and intubation with adequate depth of anesthesia and muscle relaxation. Rocuronium, succinylcholine, and atracurium all provided sufficient muscle relaxation to achieve successful intubation and no increase in IOP. However, rocuronium 0.6 mg/kg provided significantly better intubating conditions compared with atracurium, and it resulted in a significantly greater decrease in IOP compared with baseline than succinylcholine.

Adolescent↗